Long non-coding RNA H19 promotes corneal neovascularization by targeting microRNA-29c | Zendy

Baoqi Sun | Zendy; Yiheng Ding | Zendy; Xin Jin | Zendy; Shuo Xu | Zendy; Hong Zhang | Zendy

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Long non-coding RNA H19 promotes corneal neovascularization by targeting microRNA-29c

Author(s) -

Baoqi Sun,

Yiheng Ding,

Xin Jin,

Shuo Xu,

Hong Zhang

Publication year - 2019

Publication title -

bioscience reports

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.938

H-Index - 77

eISSN - 1573-4935

pISSN - 0144-8463

DOI - 10.1042/bsr20182394

Subject(s) - microrna , umbilical vein , angiogenesis , vascular endothelial growth factor a , cancer research , corneal neovascularization , fibroblast growth factor , basic fibroblast growth factor , microbiology and biotechnology , competing endogenous rna , biology , neovascularization , three prime untranslated region , vascular endothelial growth factor , in vitro , untranslated region , rna , long non coding rna , chemistry , growth factor , genetics , receptor , vegf receptors , gene

Long non-coding RNA (lncRNA) H19 has been implicated in tumor angiogenesis. However, whether H19 regulates the progression of corneal neovascularization (CNV) is unclear. The present study aimed to determine the function of H19 in CNV and its possible molecular mechanism. Here, we found that the H19 levels were remarkably increased in vascularized corneas and basic fibroblast growth factor (bFGF)-treated human umbilical vein endothelial cells (HUVECs). In vitro , H19 up-regulation promoted proliferation, migration, tube formation and vascular endothelial growth factor A (VEGFA) expression in HUVECs, and it was found to down-regulate microRNA-29c (miR-29c) expression. Bioinformatics analysis revealed that H19 mediated the above effects by binding directly to miR-29c. In addition, miR-29c expression was markedly reduced in vascularized corneas and its expression also decreased in bFGF-treated HUVECs in vitro MiR-29c targeted the 3' untranslated region (3'-UTR) of VEGFA and decreased its expression. These data suggest that H19 can enhance CNV progression by inhibiting miR-29c, which negatively regulates VEGFA. This novel regulatory axis may serve as a potential therapeutic target for CNV.

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